By Kerry Grens The rare, severe effects of Zika infection in adults may go beyond Guillain-Barre syndrome. Doctors in Brazil report today in JAMA Neurology that among a group of hospitalized patients, those with the virus sometimes presented with other neurological problems—namely, an inflamed nervous system. The physicians tracked 40 patients who came to a hospital in Rio de Janeiro between December 2015 and May 2016 for acute neuroinflammation. Among them, 35 turned out to have been infected with Zika, and within this group, 27 had Guillain-Barre syndrome, which causes debilitating paralysis. Five patients had encephalitis, or inflammation of the brain, two had inflamed spinal cords, and one had nerve inflammation. Such symptoms are thought to indicate “post-infectious syndromes, where you have a viral infection, you clear the infection by mounting an antibody response, and the antibodies actually attack parts of the central and peripheral nervous system, causing these neurological symptoms,” Richard Temes, director of the Center for Neurocritical Care at North Shore University Hospital in Manhasset, New York, tells HealthDay. He was not involved in this study. Zika infection in adults is typically not dangerous, and many people won’t develop symptoms at all. Doctors have noticed an uptick in Guillain-Barre syndrome among those who have caught the virus. The authors note in their study that admissions to their hospital for both Guillain-Barre syndrome and encephalitis rose after May 2014, when the Zika outbreak hit Brazil.

Keyword: Movement Disorders
Link ID: 23960 - Posted: 08.15.2017

By Andy Coghlan Can exercise during childhood protect you against memory loss many decades later? Exercise early in life seems to have lifelong benefits for the brain, in rats at least. “This is an animal study, but it indicates that physical activity at a young age is very important – not just for development, but for the whole lifelong trajectory of cognitive development during ageing,” says Martin Wojtowicz of the University of Toronto, Canada. “In humans, it may compensate for and delay the appearance of Alzheimer’s symptoms, possibly to the point of preventing them.” Wojtowicz’s team spilt 80 young male rats into two equal groups, and placed running wheels in the cages of one group for a period of six weeks. Around four months later – when the rats had reached middle age – the team taught all the rats to associate an electric shock with being in a specific box. When placed in the box, they froze with fear. Two weeks later, the team tested the rats in three scenarios: exactly the same box in the same room, the same box with the room arranged and lit differently, and a completely different box in a different room. The rats without access to a running wheel when they were young now froze the same proportion of times in each of these situations, suggesting they couldn’t remember which one was hazardous. But those that had been able to run in their youth froze 40 to 50 per cent less in both altered box settings. © Copyright New Scientist Ltd

Keyword: Alzheimers; Development of the Brain
Link ID: 23959 - Posted: 08.15.2017

By Kate Kyle, CBC News Widespread, prolonged hunger that existed in residential schools is a contributing factor in the disproportionate health issues facing many Indigenous people, such as diabetes and obesity, according to an article published Monday in the Canadian Medical Association Journal. "Hunger is really central to the experiences of residential school survivors," says Ian Mosby who co-authored the article with Tracy Galloway, both with the University of Toronto. They say childhood malnutrition experienced in many government-funded schools is contributing to the higher risk for obesity, diabetes and heart disease among Indigenous people in adulthood. "While this wasn't every single residential school," says Mosby, "it's common enough through survivor testimony that we need to start looking at hunger in residential schools as a real predictor of long-term health problems." Residential school kitchen 1920s Residential schools across Canada faced significant underfunding, along with inadequate cooking facilities and untrained staff. Historians and former students have described children getting "one or two pieces of stale bread for lunch. Rarely getting meat, rarely getting milk and butter, and few fruits and vegetables," says Mosby. ©2017 CBC/Radio-Canada.

Keyword: Obesity; Development of the Brain
Link ID: 23958 - Posted: 08.15.2017

By NICHOLAS BAKALAR Children who sleep less may be at increased risk for Type 2 diabetes, researchers report. Earlier studies found a link between shorter sleep and diabetes in adults, but the connection has been little studied in children. British researchers studied 4,525 9- and 10-year olds from varying ethnic backgrounds. On average, their parents reported they slept 10 hours a night, with 95 percent sleeping between eight and 12 hours. The study, in Pediatrics, found that the less sleep, the more likely the children were to have higher body mass indexes, higher insulin resistance and higher glucose readings. All three are risk factors for Type 2 diabetes. Over all, increasing weekday sleep duration by an hour was associated with a 0.2 lower B.M.I. and a 3 percent reduction in insulin resistance. The reasons for the link remain unclear, but the researchers suggest that poor sleep may affect appetite regulation, leading to overeating and obesity. This observational study could not establish cause and effect. Still, the senior author, Christopher G. Owen, a professor of epidemiology at St. George’s University of London, said that for children, the more sleep the better — there is no threshold. “Increasing sleep is a very simple, low-cost intervention,” he said. “We should be doing our utmost to make sure that children sleep for an adequate amount of time.” © 2017 The New York Times Company

Keyword: Sleep; Obesity
Link ID: 23957 - Posted: 08.15.2017

By M. GREGG BLOCHE Was the Central Intelligence Agency’s post-9/11 “enhanced interrogation” program an instance of human experimentation? Recently declassified documents raise this explosive question. The documents were obtained by the American Civil Liberties Union in connection with a federal lawsuit scheduled for trial next month. The case was brought on behalf of three former detainees against two psychologists who developed the C.I.A.’s program. I reviewed some of the documents in a recent article in The Texas Law Review. Internal C.I.A. records indicate that the psychologists, James Mitchell and John Bruce Jessen, anticipated objections that critics would later level against the program, such as that coercion might generate unreliable information, and contracted with the agency to design research tools that addressed some of these concerns. Redactions in the released documents (and the C.I.A.’s withholding of others) make it impossible to know the full extent, if any, of the agency’s data collection efforts or the findings they yielded. At their depositions for the A.C.L.U. lawsuit, each of the psychologists denied having evaluated the program’s effectiveness. But the C.I.A. paid the psychologists to develop a research methodology and instructed physicians and other medical staff members at clandestine detention sites to monitor and chart the health conditions of detainees. In response, the advocacy group Physicians for Human Rights has charged that the program was an unlawful experiment on human beings. It calls the program “one of the gravest breaches of medical ethics by United States health professionals since the Nuremberg Code,” the ethical principles written to protect people from human experimentation after World War II. In its lawsuit, the A.C.L.U. is pressing a similar claim. © 2017 The New York Times Company

Keyword: Aggression
Link ID: 23956 - Posted: 08.14.2017

By Kristine Phillips The Food and Drug Administration is investigating the sudden deaths of five people who had undergone an obesity treatment that places an inflated silicone balloon in their stomach. All deaths happened within a month of the procedure, the FDA said in a letter earlier this week to health-care providers. Three people died just one to three days later. The agency, however, cautioned that it has yet to determine whether the devices or the way in which they were placed in the stomachs directly caused those deaths. “At this time, we do not know the root cause or incidence per rate of patient death,” the FDA said, adding that it is working with the companies that manufacture the devices. The devices are manufactured by two California companies. Four of the cases involved the Orbera Intragastric Balloon System by Apollo Endosurgery. One involved the ReShape Integrated Dual Balloon System by ReShape Medical. The deaths happened from 2016 to present, according to the FDA. The agency said two more death reports it received happened within the same time frame and are potentially related to complications from the balloon treatment. The procedure lasts for up to 30 minutes. One or two balloons are placed inside the stomach through the mouth using an endoscope while a patient is mildly sedated. Once inside, it's inflated with liquid, usually with saline solution. The idea is for the balloon, which is about the size of a grapefruit once inflated, to leave less room for food. It stays in the stomach for up to six months, while the patient also follows a diet and exercises regularly. © 1996-2017 The Washington Post

Keyword: Obesity
Link ID: 23955 - Posted: 08.14.2017

By Megan Scudellari Neuropharmacology postdoc Nick DiPatrizio was stumped. His advisor, University of California, Irvine, researcher Daniele Piomelli, had discovered eight years earlier that hungry rats have high levels of endocannabinoids, endogenous molecules that bind to the same receptors as the active ingredient in marijuana. Now, in 2009, DiPatrizio was trying to identify exactly where and how those molecules were controlling food intake in rats. But under specific feeding conditions, he couldn’t locate any changes in endocannabinoid levels in the brain, which is flush with endocannabinoid receptors and the obvious place to look for behavioral signals. Piomelli gently chastised his mentee. “He said, ‘You’re being neurocentric. Remember, there’s a body attached to the head. Look in the other organs of the body,’ ” recalls DiPatrizio. So the young scientist persisted, and eventually discovered that hunger—and the taste of fat—leads to increased endocannabinoid levels in the jejunum, a part of the small intestine. Endocannabinoid signaling in the gut, not the brain, was controlling food intake in the rodents in response to tasting fats.1 The evolution of endocannabinoid research has mirrored DiPatrizio’s early thinking: ever since the first endocannabinoid receptor was identified in the late 1980s, the field has been overwhelmingly focused on the central nervous system. The main endocannabinoid receptor, CB1, was first discovered in a rat brain and is now known to be among the most abundant G protein–coupled receptors in neurons there. Plus, cannabis is well-known for its psychotropic effects. “That has led the research field to be very CNS-oriented,” says Saoirse O’Sullivan, who studies endocannabinoids at the University of Nottingham in the U.K. © 1986-2017 The Scientist

Keyword: Drug Abuse
Link ID: 23954 - Posted: 08.14.2017

Eric Deggans Like a lot of kids in high school, Sam worries that he doesn't fit in. "I'm a weirdo. That's what everyone says," declares the 18-year-old character at the center of Netflix's new dramatic comedy series Atypical. One reason Sam struggles to fit in: He has autism. As his character explains at the start of the first episode, sometimes he doesn't understand what people mean when they say things. And that makes him feel alone, even when he's not. Sam's family in Atypical is thrown in all sorts of new directions by his quest to date and find a girlfriend. Creator Robia Rashid says she wanted to tell a different kind of coming-of-age story, inspired by recent increases in autism diagnoses. "There are all these young people now who are on the spectrum, who know ... they're on the spectrum," she says. "And [they] are interested in things that every young person is interested in ... independence and finding connections and finding love." On-screen depictions of autism have come a long way since Dustin Hoffman's portrayal of Raymond Babbitt in the 1988 Oscar-winning film Rain Man. Hoffman's Babbitt focused obsessively on watching The People's Court and getting served maple syrup before his pancakes. He could also memorize half the names in a phone book in one reading and count the number of toothpicks on the floor, moments after they spilled out of the box. For Atypical, Rashid says she researched accounts of adults with autism, has several parents of autistic children working in her crew and hired an actor with autism to play a minor role. © 2017 npr

Keyword: Autism
Link ID: 23953 - Posted: 08.12.2017

An experimental drug appears to slow the progression of Niemann-Pick disease type C1 (NPC1), a fatal neurological disease, according to results of a clinical study led by researchers at the National Institutes of Health. The study appears in The Lancet. NPC1 is a rare genetic disorder that primarily affects children and adolescents, causing a progressive decline in neurological and cognitive functions. The U.S. Food and Drug Administration has not approved any treatments for the condition. The drug, 2-hydroxypropyl-beta-cyclodextrin (VTS-270), is being tested under a cooperative research and development agreement, or CRADA, between NIH and Sucampo Pharmaceuticals, Inc. In April 2017, Sucampo acquired Vtesse Inc., which previously had been developing VTS-270. “The results are very encouraging and support continued development of VTS-270 for treating NPC1,” said Forbes D. Porter, M.D., Ph.D., clinical director at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and the study’s senior author. “Compared to untreated patients we followed in an earlier study, participants who received VTS-270 scored better on a scale used to evaluate disease severity and progression, including elements such as speech, cognition and mobility.” The study was a phase 1/2a clinical trial designed to test the drug’s safety and effectiveness. A group of 14 participants, ranging from ages 4 to 23 years, received the experimental drug once a month at NIH for 12 to 18 months. Another group of three participants received the drug every two weeks for 18 months at Rush University Medical Center in Chicago.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 23952 - Posted: 08.12.2017

By MALIA WOLLAN ‘‘Don’t startle the person,’’ says Charlene Gamaldo, the medical director at the Johns Hopkins Center for Sleep. Sleepwalkers exist in a semiwakeful state and can become testy and disoriented when forced to come to full consciousness. Instead, speak to them in a quiet voice and lead them gently back to their bed. In most cases, they’ll settle easily and in the morning remember nothing of their nighttime ambulations. To determine whether you’re dealing with a sleepwalker, as opposed to, say, a night owl (or someone with another, more worrisome form of parasomnia), watch for open eyes, a blank expression, physical clumsiness and a lack of reactivity. ‘‘They look zoned out,’’ Gamaldo says. Sleepwalkers tend to perform tasks from memory, including texting, shopping online, cooking and even driving and having sex, all with a noticeably odd flair. ‘‘They may get up and eat a raw TV dinner,’’ Gamaldo says. Researchers attribute a surge in sleepwalking in the 21st century to a rise in the use of hypnosedative sleeping medications. A popular hotel chain in the United Kingdom even issued sleepwalker-care guidelines to staff members after noting a sevenfold increase in sleepwalking patrons over one year, 95 percent of whom were men wandering out of their rooms naked. Other triggers include stress, genetics, fatigue, heat and what Gamaldo calls ‘‘poor sleep hygiene,’’ or loud, overly bright bedrooms filled with TVs and digital devices. To protect a sleepwalker in your home, make it as safe and soporific as possible. Keep him or her away from stairs and sharp objects. ‘‘The bedroom should be uncluttered,’’ Gamaldo says. © 2017 The New York Times Company

Keyword: Sleep
Link ID: 23951 - Posted: 08.12.2017

By Knvul Sheikh At his psychiatric clinic in the Connecticut Mental Health Center, Albert Powers sees people every day who experience hallucinations. The condition is often a hallmark of psychosis, occurring in an estimated 60 to 70 percent of people with schizophrenia, and in a subset of those diagnosed with bipolar disorder, dementia and major depression. Auditory hallucinations are the most common type experienced. Some patients report hearing voices; others hear phantom melodies. But increasing evidence over the past two decades suggests hearing imaginary sounds is not always a sign of mental illness. Healthy people also experience hallucinations. Drugs, sleep deprivation and migraines can often trigger the illusion of sounds or sights that are not there. Even in the absence of these predisposing factors, approximately one in 20 people hear voices or see visual hallucinations at least once in their lifetimes, according to mental health surveys conducted by the World Health Organization. Whereas most researchers have focused on the brain abnormalities that occur in people suffering at an extreme end of this spectrum, Powers and his colleagues have turned their attention to milder cases in a new study. “We wanted to understand what’s common and what’s protecting people who hallucinate but who don’t require psychological intervention,” he says. Normally when the brain receives sensory information, such as sound, it actively works to fill in information to make sense of what it hears—its location, volume and other details. “The brain is a predictive machine,” explains Anissa Abi-Dargham, a psychiatrist at Stony Brook University School of Medicine, who was not involved in the new work. “It is constantly scanning the environment and relying on previous knowledge to fill in the gaps [in] what we perceive.” Because our expectations are usually accurate, the system generally works well. For example, we are able to hear the sound of running water or the murmur of a friend talking across the room and then react in an instant, Abi-Dargham says. © 2017 Scientific American,

Keyword: Schizophrenia; Hearing
Link ID: 23950 - Posted: 08.11.2017

By Aylin Woodward Two newly identified brain areas in rhesus monkeys seem to help the animals recognise familiar faces. Primates, Homo sapiens included, must be able to differentiate between faces and recognise friend from foe because social hierarchies play a large role in daily life. But exactly how primate brains deal with faces is not completely clear. One idea is that the same parts of the brain are involved in recognising both familiar and unfamiliar faces, just with varying efficiency. But Sofia Landi and Winrich Freiwald at Rockefeller University in New York have now cast doubt on that thinking. Their work shows that distinct brain areas are responsible for recognising the primates you know. Many researchers have already shown that certain areas of the temporal and prefrontal cortex are involved in unfamiliar face perception in rhesus monkey brains. Using whole-brain fMRI scans of four monkeys, Landi and Freiwald have now identified two additional brain areas that play a role not only in unfamiliar face perception but also in recognising familiar faces. The two new areas are in the anterior temporal lobe – the part of our brains above and in front of our ears. One is in the perirhinal cortex and one is in the temporal pole. These regions lit up far more when the monkeys recognised a familiar face in a photograph, as opposed to when they were presented with images of a stranger. © Copyright New Scientist Ltd.

Keyword: Attention
Link ID: 23949 - Posted: 08.11.2017

By NIRAJ CHOKSHI The photos you share online speak volumes. They can serve as a form of self-expression or a record of travel. They can reflect your style and your quirks. But they might convey even more than you realize: The photos you share may hold clues to your mental health, new research suggests. From the colors and faces in their photos to the enhancements they make before posting them, Instagram users with a history of depression seem to present the world differently from their peers, according to the study, published this week in the journal EPJ Data Science. “People in our sample who were depressed tended to post photos that, on a pixel-by-pixel basis, were bluer, darker and grayer on average than healthy people,” said Andrew Reece, a postdoctoral researcher at Harvard University and co-author of the study with Christopher Danforth, a professor at the University of Vermont. The pair identified participants as “depressed” or “healthy” based on whether they reported having received a clinical diagnosis of depression in the past. They then used machine-learning tools to find patterns in the photos and to create a model predicting depression by the posts. They found that depressed participants used fewer Instagram filters, those which allow users to digitally alter a photo’s brightness and coloring before it is posted. When these users did add a filter, they tended to choose “Inkwell,” which drains a photo of its color, making it black-and-white. The healthier users tended to prefer “Valencia,” which lightens a photo’s tint. Depressed participants were more likely to post photos containing a face. But when healthier participants did post photos with faces, theirs tended to feature more of them, on average. © 2017 The New York Times Company

Keyword: Depression
Link ID: 23948 - Posted: 08.11.2017

Thomas Cronin We humans are uncommonly visual creatures. And those of us endowed with normal sight are used to thinking of our eyes as vital to how we experience the world. Vision is an advanced form of photoreception – that is, light sensing. But we also experience other more rudimentary forms of photoreception in our daily lives. We all know, for instance, the delight of perceiving the warm sun on our skin, in this case using heat as a substitute for light. No eyes or even special photoreceptor cells are necessary. But scientists have discovered in recent decades that many animals – including human beings – do have specialized light-detecting molecules in unexpected places, outside of the eyes. These “extraocular photoreceptors” are usually found in the central nervous system or in the skin, but also frequently in internal organs. What are light-sensing molecules doing in places beyond the eyes? Vision depends on detecting light All the visual cells identified in animals detect light using a single family of proteins, called the opsins. These proteins grab a light-sensitive molecule – derived from vitamin A – that changes its structure when exposed to light. The opsin in turn changes its own shape and turns on signaling pathways in photoreceptor cells that ultimately send a message to the brain that light has been detected. © 2010–2017, The Conversation US, Inc.

Keyword: Biological Rhythms; Vision
Link ID: 23947 - Posted: 08.11.2017

by Anika Burgess Art and science are often treated as distinct realms, but sometimes they overlap in unexpected ways. A neuroscientist, for example, creates a chart based on how an animal’s brain responds to rewards. The chart is informative to scientists who can interpret it—but it is also a compelling, monochrome image reminiscent of an iconic album cover. That neuroscientist is named Sean Cavanagh, of University College London, and his artwork based on the neural responses of rhesus macaques, called Unknown Variability, won the 2017 Art of Neuroscience competition. This competition has been held each year since 2011 by the Netherlands Institute for Neuroscience (NIN). NIN has existed in one form or another since the early 1900s and carries out research into brain function. Recently, the competition has opened up to include artists and their own interpretations of the brain. We know a great deal more about how the mind works than we did when NIN was founded, but there are still gaps in our understanding. Artificial intelligence is being taught to appreciate, and even create, art, for example, but the biological nature of creativity remains at the edge of our knowledge. This competition both provides scientists with the opportunity to tap into their inner Dalí, Miró, or Pollock, and offers a visual representation of research into the mysteries of thought and behavior. For the nonscientist, it might be difficult to understand “somato-dendritic morphology,” but it’s easy to appreciate its beauty when it is represented as a multicolored mosaic. © 2017 Atlas Obscura.

Keyword: Brain imaging
Link ID: 23946 - Posted: 08.11.2017

By Kai Sinclair It’s hard to see underwater, and not just because of the chlorine. The image-producing light rays that enter our eyes have trouble bending and focusing when the water’s density is almost same as that of eye fluid. Sea creatures experience the same problem, but squid use a type of lens notorious for blurry images to correct that, researchers report today in Science. Spherical lenses, like the squids’, usually can’t focus the incoming light to one point as it passes through the curved surface, which causes an unclear image. The only way to correct this is by bending each ray of light differently as it falls on each location of the lens’s surface. S-crystallin, the main protein in squid lenses, evolved the ability to do this by behaving as patchy colloids—small molecules that have spots of molecular glue that they use to stick together in clusters. The S-crystallins feature a pair of loops that act as the proteins’ sticky patches and attract the loops of other S-crystallins. Globs of six proteins link together during the squid’s larval stage and form a gel that eventually becomes the center of the lens. As the gel becomes too dense with protein clumps, smaller particles struggle to diffuse through, and a new layer of protein packages forms with just under six S-crystallins in each clump. The process continues until the outer edge of the lens is formed with pairs of S-crystallins. This allows light rays to bend a little differently in each region of the lens, which yields a clearer image. Some fish eyes are nearly identical to squids’, but it’s unknown whether their eye proteins exhibit patchy colloidlike behavior. Other cephalopods, like octopuses and nautiluses, lack S-crystallin lens proteins. So they, unlike squid, likely have blurry vision. © 2017 American Association for the Advancement of Science

Keyword: Vision; Evolution
Link ID: 23945 - Posted: 08.11.2017

Kerri Smith Marta Zlatic owns what could be the most tedious film collection ever. In her laboratory at the Janelia Research Campus in Ashburn, Virginia, the neuroscientist has stored more than 20,000 hours of black-and-white video featuring fruit-fly (Drosophila) larvae. The stars of these films are doing mundane maggoty things, such as wriggling and crawling about, but the footage is helping to answer one of the biggest questions in modern neuroscience: how the circuitry of the brain creates behaviour. It's a major goal across the field: to work out how neurons wire up, how signals move through the networks and how these signals work together to pilot an animal around, to make decisions or — in humans — to express emotions and create consciousness. Even under the most humdrum conditions — “normal lighting; no sensory cues; they're not hungry”, says Zlatic — her fly larvae can be made to perform 30 different actions, including retracting or turning their heads, or rolling. The actions are generated by a brain comprising just 15,000 neurons. That is nothing compared with the 86 billion in a human brain, which is one of the reasons Zlatic and her teammates like the maggots so much. “At the moment, really, the Drosophila larva is the sweet spot,” says Albert Cardona, Zlatic's collaborator and husband, who is also at Janelia. “If you can get the wiring diagram, you have an excellent starting point for seeing how the central nervous system works.” © 2017 Macmillan Publishers Limited

Keyword: Brain imaging
Link ID: 23944 - Posted: 08.10.2017

By Michael Price Anthropologists have waited decades to find the complete cranium of a Miocene ape from Africa—one that lived in the hazy period before the human lineage split off from the common ancestors we share with chimpanzees some 7 million years ago. Now, scientists in Kenya have found their prize at last: an almost perfectly preserved skull roughly the size of a baseball. The catch? It’s from an infant. That means that although it can give scientists a rough idea of what the common ancestor to all living apes and humans would have looked like, drawing other meaningful conclusions could be challenging. “This is the sort of thing that the fossil record loves to do to us,” says James Rossie, a biological anthropologist at the State University of New York in Stony Brook who wasn’t involved with the study. “The problem is that we learn from fossils by comparing them to others. When there are no other infant Miocene ape skulls to which to make those comparisons, your hands are tied.” The remarkably complete skull was discovered in the Turkana Basin of northern Kenya 3 years ago. As the sun sank behind the Napudet Hills west of Lake Turkana, primate paleontologist Isaiah Nengo of De Anza College in Cupertino, California, and his team started walking back to their jeep. Kenyan fossil hunter John Ekusi raced ahead to smoke a cigarette. Suddenly he began circling in place. When Nengo caught up, he saw a dirt-clogged eye socket staring up at him. “There was this skull just sticking out of the ground,” Nengo recalls. “It was incredible because we had been going up and down that path for weeks and never noticed it.” © 2017 American Association for the Advancement of Science.

Keyword: Evolution
Link ID: 23943 - Posted: 08.10.2017

By Aggie Mika Individuals who possess an innate resilience to age-related brain pathologies may offer molecular clues to unexplored therapeutics for neurodegenerative disease. After having accidentally discovered rapid aging and disease in mice with mutations in the gene that encodes the protein klotho—named after the Greek Fate Clotho, daughter of Zeus and spinner of the thread of life—independent researchers have shown that some people with genetic variants that promote elevated klotho levels live longer and tend to stave off age-related cognitive decline. In a paper published today (August 8) in Cell Reports, scientists report that a fragment of klotho, similar to what winds up in circulation after cleavage from the cell membrane, boosted spatial and short-term memory in young and aging mice and improved both memory and mobility in a transgenic mouse model of neurodegenerative disease. Notably, in each type of mouse, the protein fragment was injected into the animals’ bodies either a day or a few hours before cognitive testing took place. Previously, neurologist and researcher Dena Dubal of the University of California, San Francisco, and others have demonstrated that transgenic overexpression of klotho throughout an organism’s lifespan produces similar cognitive improvements. Dubal’s current work, she says, provides a promising answer to a “big, burning question” of klotho’s therapeutic utility: “could you give it acutely, and would it increase cognition in a rapid way?” © 1986-2017 The Scientist

Keyword: Alzheimers
Link ID: 23942 - Posted: 08.10.2017

Conor Friedersdorf This week, headlines across a diverse array of media outlets proclaimed that at least one Google employee was so antagonistic to women that he circulated a 10-page “anti-diversity screed.” That is how Gizmodo characterized the now infamous internal memo when publishing it Saturday. Similar language was used in headlines at Fox News, CNN, ABC News, the BBC, NBC News, Time, Slate, Engadget, The Huffington Post, PBS, Fast Company, and beyond (including a fleeting appearance in a headline here at The Atlantic). But love or hate the memo, which makes a number of substantive claims, some of which I regard as wrongheaded (and which would’ve benefitted greatly from an editor with more emotional intelligence than the author to help him avoid alienating his audience, even if he was determined to raise all of the same arguments), the many characterizations of the memo as “anti-diversity” are inaccurate. Using that shorthand is highly misleading. As many who read past the headlines would later observe, its author, who was later fired, began, “I value diversity and inclusion, am not denying that sexism exists, and don’t endorse using stereotypes. When addressing the gap in representation in the population, we need to look at population level differences in distributions. If we can’t have an honest discussion about this, then we can never truly solve the problem.” The balance of his memo argues that he is not against pursuing greater gender diversity at Google; he says it is against the current means Google is using to pursue that end and the way the company conceives of tradeoffs between the good of diversity and other goods. (c) 2017 by The Atlantic Monthly Group.

Keyword: Sexual Behavior
Link ID: 23941 - Posted: 08.10.2017